LPS promotes the progression of sepsis by activation of lncRNA HULC/miR-204-5p/TRPM7 network in HUVECs.
Apoptosis
/ drug effects
Case-Control Studies
Cells, Cultured
Female
Gene Expression Regulation
Human Umbilical Vein Endothelial Cells
/ drug effects
Humans
Inflammation Mediators
/ metabolism
Lipopolysaccharides
/ pharmacology
Male
MicroRNAs
/ genetics
Middle Aged
Oxidative Stress
/ drug effects
Protein Serine-Threonine Kinases
/ genetics
RNA, Long Noncoding
/ genetics
Sepsis
/ blood
Signal Transduction
TRPM Cation Channels
/ genetics
HULC
LPS
TRPM7
miR-204-5p
sepsis
Journal
Bioscience reports
ISSN: 1573-4935
Titre abrégé: Biosci Rep
Pays: England
ID NLM: 8102797
Informations de publication
Date de publication:
26 06 2020
26 06 2020
Historique:
received:
11
03
2020
revised:
31
05
2020
accepted:
01
06
2020
pubmed:
3
6
2020
medline:
23
3
2021
entrez:
3
6
2020
Statut:
ppublish
Résumé
Sepsis is a systemic inflammatory response syndrome caused by infection. Lipopolysaccharide (LPS) has been reported to induce inflammatory responses, and long non-coding RNA highly up-regulated in liver cancer (HULC) expression was associated with the progression of sepsis. But the role and underlying mechanism of HULC in LPS-induced sepsis remain unclear. Cell viability and apoptosis were measured by methyl thiazolyl tetrazolium (MTT) and flow cytometry assays, respectively. The levels of apoptosis-related proteins, inflammatory cytokines and transient receptor potential melastatin7 (TRPM7) were detected by western blot. Reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA) levels were detected by dichloro-dihydro-fluorescein diacetate (DCFH-DA) method using commercial kit. HULC, microRNA-204-5p (miR-204-5p) and TRPM7 expressions in serum of sepsis patients and human umbilical vein endothelial cells (HUVECs) were examined by quantitative real-time polymerase chain reaction (qRT-PCR). Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to confirm the interaction between HULC and miR-204-5p, miR-204-5p and TRPM7. LPS stimulation restrained cell viability and facilitated apoptosis, inflammatory injury and oxidative stress in HUVECs. HULC and TRPM7 were increased and accompanied with decreased miR-204-5p expression in serum of sepsis patients. A significant negative correlation between miR-204-5p and HULC or TRPM7 was observed, and there was a positive relationship between expressions of HULC and TRPM7. Importantly, LPS inhibited the cell viability and induced apoptosis, inflammatory injury and oxidative stress of HUVECs by up-regulating the expressions of HULC and TRPM7, and down-modulating miR-204-5p expression. Mechanically, HULC positively regulated TRPM7 expression by sponging miR-204-5p in HUVECs. LPS impaired cell viability, and promoted cell apoptosis, inflammatory response and oxidative stress in HUVECs by regulating HULC/miR-204-5p/TRPM7 axis.
Identifiants
pubmed: 32484206
pii: 225116
doi: 10.1042/BSR20200740
pmc: PMC7295636
pii:
doi:
Substances chimiques
HULC long non-coding RNA, human
0
Inflammation Mediators
0
Lipopolysaccharides
0
MIRN204 microRNA, human
0
MicroRNAs
0
RNA, Long Noncoding
0
TRPM Cation Channels
0
Protein Serine-Threonine Kinases
EC 2.7.11.1
TRPM7 protein, human
EC 2.7.11.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2020 The Author(s).
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